Alopecia areata (AA) is an immune-mediated, nonscarring hair loss with established associations with various autoimmune conditions, including inflammatory bowel disease. The following case describes a 38-year-old White male patient with Crohn's disease who developed rapidly-progressive alopecia areata during treatment with infliximab. Despite discontinuation of infliximab and aggressive treatment with corticosteroids and tofacitinib, the patient progressed to alopecia universalis within six months. Concurrently, the patient's Crohn's disease required escalation to colectomy with ostomy placement due to inadequate response to vedolizumab. Following his colectomy, the patient continued treatment with tofacitinib and demonstrated dramatic improvement in his AA, achieving complete hair regrowth within one year and maintaining remission two years after discontinuation of all immunosuppressive therapies. This case illustrates potential mechanistic connections between alopecia areata and Crohn's disease through shared inflammatory pathways involving interferon-γ and JAK signaling. The temporal relationship between the patient's colectomy and remission of his alopecia areata suggests a gut-immune axis mechanism, where addressing the primary intestinal inflammatory source may have influenced a remote autoimmune manifestation. This case highlights the potential for targeting primary inflammatory sources to achieve broader immunologic benefits in patients with concurrent autoimmune conditions.
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